This proposal seeks to elucidate the mechanisms regulating the altered reactivity of skeletal muscle arterioles to oxygen levels and vasodilator stimuli that occurs during hypertension and during elevated dietary salt intake in normotensive. The time course, mechanisms, and reversibility of salt- and hypertension-induced changes in the arteriolar reactivity will be assessed by measurements of vessel diameter, arteriolar blood flow, and vascular smooth muscle transmembrane potential during changes in oxygen availability or the application of vasodilator agonists in the rat cremaster muscle. Further, the effects of hypertension and elevated salt intake on tissue oxygenation patterns will be asses with oxygen microelectrodes in the cremaster muscle at rest, during maximal vasodilation, and under conditions of elevated oxygen demand produced by muscle stimulation. The role of angiotensin II (AngII) in contributing to altered microvascular reactivity and tissue oxygenation patterns will be assessed in rats receiving a continuous infusion of AngII with and without blockade of the specific receptor subtypes in the microcirculation. The proposed studies should provide important insight into the mechanisms of peripheral vascular alterations in salt sensitive hypertension.